Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0079731 (B-cell lymphoma)
 16,671 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Murine B cell growth factor II (BCGF-II/interleukin 5) was purified from the conditioned media of the helper T cell line D10 . G4 . 1. The purification scheme consisted of sequential batch adsorption onto trimethylsilyl-controlled pore glass beads, high pressure ion exchange chromatography, and reverse phase high pressure liquid chromatography. The purified BCGF-II had a relative molecular weight of 45,000 when analyzed by sodium dodecyl sulfate-polyacrylamide gel electrophoresis under nonreducing conditions. Identical analysis of BCGF-II under reducing conditions yielded a m.w. of 22,500, suggesting that native BCGF-II exists as a homodimer. The NH2-terminal amino acid sequence of the purified lymphokine was determined by automated Edman degradation. A single amino acid sequence of 24 residues was obtained that, upon comparison, was contained within the cDNA pSP6K-mTRF23 recently described as encoding murine BCGF-II/T cell-replacing factor. The NH2-terminal methionine in mature BCGF-II is found at position 21 of the amino acid sequence predicted from the cDNA pSP6K-mTRF23. This finding supports the contention of Kinashi et al. (Kinashi, T., N. Harada, E. Severinson, T. Tanabe, P. Sideras, M. Konishi, C. Azuma, A. Tominaga, S. Bergstedt-Lindqvist, M. Takahashi, F. Matsuda, Y. Yaoita, K. Takatsu, and T. Honjo. 1986. Nature 324:70) that amino acids 1-20 serve as the signal sequence for the BCGF-II gene. The ability of BCGF-II to stimulate the proliferation of the B cell lymphoma BCL1 was used to assess the potency of the lymphokine. BCGF-II at 13.5 pM induced 50% of the maximal proliferative response in the BCL1 cells; concentrations as low as 2 pM were still effective in stimulating the growth of the cells. Assuming that the amount of BCGF-II necessary to mount a 50% response in the BCL1 assay is defined as one unit of activity, then the purified BCGF-II has a specific activity of 16.5 U/ng of protein.
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PMID:Purification and partial sequence analysis of murine B cell growth factor II (interleukin 5). 349 67

Cross-linking of membrane Ig receptors by anti-mu antibodies (Ab) or treatment with ionomycin induced complete growth arrest and subsequent apoptotic cell death in an immature B cell lymphoma, BKS-2. The growth-inhibitory signals delivered by anti-mu and ionomycin were overcome by anti-CD3-activated Th2 clones D10.G4 and F1 and by Th1 cell clone S53. In this report the Th-mediated growth reversal in BKS-2 cells was shown to require contact-dependent interactions when the inhibition was caused by immobilized anti-mu or ionomycin. Th2 cells in transwells (lymphokines) failed to protect BKS-2 cells from the growth-inhibitory effect of immobilized anti-mu or ionomycin. Monoclonal antibodies to CD5 or CD40 ligands on activated Th cells partially inhibited the Th2 contact-dependent growth reversal of BKS-2 cells whereas simultaneous addition of both antibodies effectively prevented the delivery of contact-mediated growth signal. In contrast, anti-class I or class II Ab did not affect Th cell mediated growth reversal of BKS-2 cells. These data demonstrated that noncognate physical interaction with Th cells was essential for the recovery of BKS-2 cells when the latter were growth-arrested by strong inhibitory stimuli such as immobilized anti-mu and ionomycin. Further CD5 as well as CD40 ligands on Th cells are important for signal transduction in this type of T-B interaction.
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PMID:Involvement of CD5 in Th1 and Th2 contact-mediated rescue of anti-mu and ionomycin induced growth inhibition in a B cell lymphoma. 753 38

In human T cells CD45 is reported to associate with both cell surface and intracellular molecules including CD2, CD4/CD8, CD5, p56lck and p59fyn. In this study the association of molecules with CD45 in murine T lymphocytes was explored using biotinylation, chemical cross-linking, immunoprecipitation and 32P-labelling. Sodium dodecyl sulphate-polyacrylamide gel electrophoresis (SDS-PAGE) analysis of CD45 monoclonal antibody (mAb) (S-450-15.2) immunoprecipitates from Triton X-100 lysates of murine thymocytes that were surface biotinylated and treated with the chemical cross-linker 3,3'-dithio-bis(sulpho-succinimidylpropionate) (DTSSP) showed that CD45 can be chemically linked to molecules of 25,000-32,000, 42,000 and 60,000-70,000 MW. The CD45 mAb also co-precipitated a prominent 32,000 MW molecule from digitonin lysates of surface biotinylated murine thymocytes, splenocytes and D10 cells, but a weaker association was also detected on splenic B cells and on the murine B-cell lymphoma line A20. The results suggest that in these cells CD45 is associated with a 32,000 MW molecule which is exposed extracellularly. Experiments in which thymocytes were biotinylated after permeabilization with lysolecithin showed that additional molecules of 33,000, 55,000, 60,000 and 90,000 MW, presumably localized intracellularly, also co-precipitated with CD45. Labelling of murine thymocytes or D10 cells with H3(32)PO4 in vivo, and of CD45 immunoprecipitates by in vitro kinase reaction, revealed that the 32,000-33,000 MW molecules are phosphoproteins. The relationship of these molecules with the 30,000-34,000 MW molecules previously reported to associate with CD45 in human T cells is not clear as a number of differences were observed. Firstly, the molecular weight of the CD45-associated 32,000-33,000 MW molecule(s) on murine T cells and B cells is slightly lower than that observed in the human T-cell line Jurkat (34,000 MW). Secondly, phosphoamino acid analysis after in vitro kinase labelling of CD45 immunoprecipitates showed that the murine 32,000-33,000 MW molecules are phosphorylated exclusively on serines. Thirdly, although in vitro phosphorylation of the 32,000-33,000 MW molecules was inhibited by preincubation with either GTP-gamma-S or GDP-beta-S, the 32,000-33,000 MW CD45-associated molecules did not bind 32P-GTP, GDP-agarose, or react with antisera to a consensus sequence of G proteins. The crucial role of CD45 for proper function of the T-cell receptor (TCR), suggests that the CD45-associated 32,000-33,000 MW molecules and kinases also may play a role in the signalling events leading to T-cell activation.
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PMID:Evidence for an association of CD45 with 32,000-33,000 MW phosphoproteins on murine T and B lymphocytes. 783 67

Malignant lymphomas represent about 9% of cardiac neoplasms. Despite its life-threatening nature, the cardiac manifestations are often subclinical. In about 20% of deaths from lymphoma, cardiac involvement is found only in autopsy. The authors present the case of a 77-year-old female admitted due to intense back pain, vomiting, generalised pruritus, fatigue and weight loss. She had a personal history of hypertension and breast cancer was noted 10 years before admission. The thoracoabdominopelvic CT showed a mass in the left atrium with extension to the right atrium and inferior vena cava, and a paravertebral mass at D10-D11 with invasion of the spinal canal and hepatic hilum. The transthoracic paravertebral mass biopsy was compatible with a diffuse large B cell lymphoma. The patient developed a complete atrioventricular block, with haemodynamic instability, requiring urgent chemoreduction of the paracardiac mass and implantation of an epicardial pacemaker.
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PMID:Complete heart block as a complicating feature of a mediastinal lymphoma. 2260 4

Maspin has been identified as a tumor suppressor gene in breast cancer, but the underlying regulatory mechanisms remain unclear. In the present study, maspin pcDNA was transfected into MCF-7 cells. microRNA (miR) microarray and reverse transcription-quantitative polymerase chain reaction was used for analysis; the results demonstrated that maspin may inhibit miR-10b, miR-21 and miR-451 expression in MCF-7 cells. In addition, maspin increased the expression of certain miR-21 target genes (phosphatase and tensin homolog, programmed cell death 4 and B-cell lymphoma-2), miR-10b target gene (Homeobox D10; HOXD10) and miR-451 target gene (multidrug resistance protein 1). Furthermore, the results of the present study revealed that decreased expression of miR-21 suppressed the invasion and proliferation of MCF-7 cells. Therefore, in the present study, it was hypothesized that as a tumor-suppressor gene, the potential molecular mechanism of maspin include down-regulating the expression of miR-21 and increasing the expression of specific miR-21 target genes.
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PMID:Maspin inhibits MCF-7 cell invasion and proliferation by downregulating miR-21 and increasing the expression of its target genes. 3221 12